A 65-year-old man was admitted to the ICU after sustaining lower limb fractures in a motorcycle crash that required prolonged surgery. He developed significant blood loss and increased oxygen needs during the operation. Upon arrival in the ICU, his blood gas showed low oxygen levels. The document discusses the principles and rationale for hemostatic resuscitation in trauma patients with significant bleeding, including rapidly correcting hypothermia, acidosis, and coagulopathy through a balanced transfusion of blood products while limiting crystalloid fluids. It emphasizes the importance of achieving hemostasis and avoiding dilutional coagulopathy.

1. Dr Santosh Kumar Bhaskar
Professor Anaesthesiology
Chirayu Medical College
Haemostatic Resuscitation

2. A 65-year-old male with a past history of ischaemic
heart disease is admitted to the ICU after a
motorcycle crash having sustained long bone
fractures of the lower limbs. He has no head, chest
or abdominal injuries.
Prior to surgery, his Glasgow Coma Scale (GCS) was
15 and Sp02 was 98% on 4 L/min oxygen via a
Hudson mask, and chest X-ray was normal. He
required prolonged operative fixation of his
fractures and that was complicated by significant
blood loss. Intra-operatively, he also developed an
increasing oxygen requirement.
On arrival in ICU, his most recent arterial blood gas,
taken on a Fi02 of 0.7 shows Pa02 of 55 mmHg (7.3
kPa).

4. Definition of hemostatic
resuscitation
 Rapid correction of haemostasis-
impairing factors, such as
hypothermia hypocalcemia and
acidosis
 Resuscitation with a balanced
combination of blood products,
which in combination resemble the
composition of whole blood, aiming
to avoid dilutional coagulopathy.

5. resuscitation:
 Reverse hypothermia
 Reverse acidosis
 Limit crystalloid load
 Use blood components in a proportion
which resembles whole blood
 Reverse fibrinolysis associated with
massive blood loss
 Achieve this whole-blood-like ratio within
the first 6 hours of resuscitation

6. Rationale for aggressive correction
of coagulopathy
 Exsanguination is a major cause of death
in trauma (40% of trauma-related death in
the first 24 hours is due to haemorrhage)
 Coagulopathy is common: 25% of severe
trauma patients are coagulopathic at
presentation
 According to retrospective cohort studies
(MacLeod et al, 2003) and the
coagulopathic patients have increased
mortality (46%) compared to non-
coagulopathic controls (11%).

7. Rationale for avoiding large
volumes of crystalloid
 Aggressive resuscitation with crystalloid leads to
haemodilution.
 Haemodilution decreases the concentration of clotting
factors and leads to coagulopathy.
 75% of the crystalloid volume load distributes into the
extravascular space; organ and tissue oedema
ensues, putting the patient at risk of pulmonary
oedema and abdominal compartment syndrome
(among other problems).
 Crystalloids do not contribute to the transport of
oxygen; by diluting the blood they actually decrease
its oxygen-carrying capacity.
 In the case of saline, crystalloid resuscitation may
exacerbate the acidosis.

8. Rationale for using a balanced
blood product ratio
 Transfusion of packed red cells does not restore
clotting factors.
 Coagulopathy will develop if packed red cells are the
sole resuscitation fluid.
 Transfused PRBCs suffer from storage lesions. Their
oxygen-carrying capacity isn't very good anyway.
 The citrate in the PRBCs tends to chelate the patient's
calcium; this can't be good for their clotting function.
 It stands to reason that whole blood is the best
resuscitation fluid to replace whole blood which is lost
by haemorrhage.
 A "balanced" ratio of blood products resembles whole
blood.
 The precise ratio of platelets plasma and PRBCs is
still being debated.

9. Rationale for correction of
acidosis
 Nonsurvivors of trauma are more likely to have
been acidotic than survivors
 Acidosis in trauma is largely the consequence of
raised lactate
 The lactate is generated not only by tissue
anaerobic metabolism, but also by the β-agonist
adrenergic effects of endogenous
catecholamines.
 The main problems with acidosis in trauma is its
influence on coagulopathy and haemodynamic
performance (Lier et al, 2008). In fact, acidosis
seems to be more important for coagulopathy
than the hypothermia (Hoffman et al, 2004)

10. Coagulopathy due to acidosis is the
result of multiple pathophysiological
processes
 The main problem is impaired thrombin generation.
The thrombin generation rate during the propagation
phase is impaired by 50% at a pH of 7.10.
 Platelet structure changes at a pH below 7.4: they
assume a spherical shape, and lose their
pseudopodia.
 Clotting factors function poorly -particularly Factors V,
VIIa and X- because the interaction between the
clotting factors and negatively charged phospholipids
is impaired at low pH (Hess et al, 2006).
 Decreased availability of ionised calcium (due to the
change in its protein binding dynamics)- therefore,
poor clotting function.
 Clotting factors which require iCa2+ have a decreased
affinity for it at a low pH.

11.  The haemodynamic effects of metabolic
acidosis are also counterproductive, particularly if
the pH is below 7.10:. Specific problems are
listed as follows.
Decreased cardiac output
Increased propensity to arrhythmias
Decreased systemic vascular tone
and arterial vasodilation
Decreased responsiveness to
catecholamines
Pulmonary vasoconstricition

12. Rationale for correcting
hypothermia
 Hypothermia seems to have a real impact on
trauma outcomes: in a retrospective analysis of
trauma patients (Jurkovich et al, 1987), the
temperature was associated with the following
mortality rates:
 Presenting temperature of over 34°C =
mortality of 7%;
 33-34°C = mortality of 40%;
 32-33°C = mortality of 67%,
 Under 32°C = mortality of 100%,

13. Effects
 In short, at 33°C the clotting activity is
suppressed to the point where it resembles a
50% reduction in clotting factor concentration
(even when the actual concentration is normal).
Interestingly, recombinant Factor VIIa
(Novoseven) still retains its activity at 34°C (+/-
2.5°C).
 Platelet activity is also impaired at low
temperature;Each 1°C decrease in temperature
results in a 15% decrease in the rate of
thromboxane B2 production (thus, platelet

14. Rationale for correction of
fibrinolysis with tranexamic acid
 One of the effects of trauma is to induce
a hyperfibrinolytic state
 The major source of this seem to be
increased serum levels of
thrombomodulin and tPA (Brohi et al,
2008)
 It would therefore make sense to give a
tPA inhibitor such as tranexamic acid or
eta-aminocaproic acid

15. Rationale for the use of
hypertonic saline
 After the resuscitation of trauma, massive tissue injury
and ischemia/reperfusion produces an exaggerated
systemic inflammatory response syndrome (SIRS) .
 Extravasation and sequestration of neutrophils into
vital organs is one of the main mechanisms of organ
damage in this context
 Hypertonic saline is said to have immunomodulatory
effects, specifically affecting neutrophil migration
(Angle et al, 2000) and decreasing the permeability of
the blood-brain barrier.
 As a hyperosmolar solution, it should theoretically
expand the volume of extracellular fluid by osmotically
"borrowing" water from the intracellular compartment-

16. Problems with haemostatic
resuscitation
 The ideal resuscitation fluid
would of course be whole blood.
Unfortunately, this is usually not
available. One may try to
recombine stored blood products
to achieve an end result which
resembles whole blood, but it is
never quite the same due to
lesions of processing and
storage.

17.  All blood products suffering storage
lesions are cold (contributing to
hypothermia) and acidic (because of
cellular metabolism in storage, as
well as due to citrate-based storage
media)
 The infusion of massive amounts of
blood products exposes the patient
to risks of massive transfusion which
are not trivial, and it is debatable
whether these risks outweigh the risks
of massive crystalloid load

18.  Tranexamic acid may have
prothrombotic effects which increase
the risk of DVT in already DVT-prone
trauma patients. Furthermore, the
methodology of the major trial in
support of its use makes it difficult to
generalise its finding to the ICU
setting

19.  Hypertonic saline can theoretically increase
the risk of bleeding by causing some sort of
platelet function impairment (fortunately
studies have demonstrated that one would
need to replace 10% of their blood volume
with hypertonic saline before one experiences
any of these effects).

20. Take home message
 Immediate resuscitation:
 Primary survey should include the
assessment of core temperature.
 Haemostasis by direct pressure wherever
this is possible
 ABG to determine the pH, lactate,
haemoglobin level and ionised calcium
 Activate the massive transfusion protocol in
liason with local blood bank and haematology
service

21. Take home message
 Organise transfusion: 1:1:1 FFP, platelets,
PRBCs.
 Haemoglobin level is not a valid transfusion
trigger, nor can transfusion wait for
haemoglobin levels to become available.
 Any transfused blood products should be
warmed with a heater. Six units of RBCs at
4ºC will reduce the body temperature of an
average 70 kg adult by 1ºC.
 Crystalloid is to be avoided unless there is
no other option and haemodynamic
performance if life-threateningly poor

22. Take home message
 Tranexamic acid 1g over 10
minutes
 Correct ionised calcium
 Commence warming the patient
externally
 Practice permissive hypotension is
permitted by the absence of
neurotrauma
 Within the first 6 hours:

23. Take home message
 Coags data, plus/minus TEG or ROTEM (its
utility and cost effectiveness over traditional
coags is still being questioned) will guide the
ongoing use of blood products.
 Tranexamic acid 1g over 8 hours to chase the
first dose (as per CRASH-2 protocol)
 Cryoprecipitate 3-4g should be given if the
fibrinogen level is below 1.0
 Recombinant Factor VIIa (Novoseven) should
be thought about if the coags are trending
towards normal, and the patient is still
exsanguinating (the dose should be 90 μg/kg)

24. Thanks for
patients
hearing